The work propose will define some of the interactions of several plasma enzyme systems involved in coagulation, fibrinolysis, kinin release, and in complement function as they participate in reactions to injury to maintain the patency and integrity of the blood vessels. Certain kininogens are essential to normal coagulation of plasma, and are sources of polypeptide kinins which can cause signs of inflammation. Kininogens will be quantified immunologically to compare their concentrations in plasma from normal persons with that in certain disorders. Kininogens will also be identified in tissues by an immunofluorescence technique. The manner in which surface-initiated clotting activity enhanced activation of the first component of complement (C1) in plasma from persons with hereditary angioneurotic edema (HANE) will be explored by testing the ability of chromatographically purified preparations of Hageman factor and plasma proteins which depend upon Hageman factor for their activity to then activate preparations of C1. This should determine if C1 can be activated only through the activation of plasminogen. Serum inhibitor of activated C1 also inhibits several hemostatic enzymes. To determine if all of its inhibitory functions depend upon the same structural properties of this inhibitor, abnormal forms of this protein from plasma of persons with HANE associated with non-functional inhibitors will be isolated and tested for their capacity to inhibit preparations of plasmin (a fibrinolytic enzyme), activated Hageman factor (a clotting enzyme), and plasma kallikrein (a kinin-releasing enzyme). In preliminary work aimed to examine the role of a distinctive polypeptide kinin from HANE plasma in normal person, antibody to this kinin will be prepared and characterized.